OBJECTIVE: This study investigated the relationship between adiposity, lifetime physical activities and serum adiponectin as breast cancer risk factors among Malaysian women in Klang Valley, Malaysia.
DESIGN: A case-control study was carried out among 70 newly diagnosed breast cancer patients and 138 controls aged 29 to 65 years old in Klang Valley.
SUBJECTS: The inclusion criteria for both groups were not having menstruation for premenopausal women, no evidence of pregnancy, not lactating and no chronic diseases such as hypertension and diabetes at the time of data collection. In addition, the cases must be pathologically newly diagnosed with breast cancer (stage I to III) and not on any therapy for cancer, with the exception of surgery. The controls were matched with cases for age +/- 5 years and menopausal status.
MEASUREMENTS: Subjects were interviewed to obtain information on socio-demography, health and reproductive history using a pretested questionnaire. Subjects were also asked on their engagement of physical activity since secondary school. Anthropometric parameters included height, weight, waist and hips were also measured. A total of 6 ml of fasting venous blood was drawn for analysis of serum adiponectin in duplicate using Linko Adiponectin ELISA Kit. Fasting blood glucose (FBG) and blood pressure were also measured.
RESULTS: Mean body mass index (BMI) among cases and controls were not significantly different (p> 0.05) at 26.1 -/+ 4.8 kg/m2 and 25.3 -/+ 4.5 kg/m2, respectively. FBG among cases (6.3 -/+ 1.8 mmol/L) was higher than controls (5.6 -/+ 1.1 mmol/L) (p<0.05). Waist hip ratio (WHR) of cases (0.85 -/+ 0.07) was also higher than controls (0.80 -/+ 0.06) (p<0.05). Abdominal obesity (WHR > 0.85) increased risk of breast cancer by three folds [Adjusted OR 3.3 (95%CI 1.8-6.2)] (p<0.05). Adiponectin level was inversely related to waist circumference (r=-0.510, p=0.000), BMI (r=-0.448, p=0.000) and FBG (r=-0.290, p=0.026). Adiponectin level in cases (11.9 -/+ 4.8 microg/ml) were lower than controls (15.2 -/+ 7.3 microg/ml) (p<0.05). A greater reduction of breast cancer risk was observed with the increasing level of serum adiponectin level according to percentiles (p<0.05). Subjects with mean serum adiponectin level at the highest quintile (> 75th)( >or= 16.7 microg/ml) had 80% reduced risk of breast cancer [Adjusted OR 0.2 (0.0-0.6)](p<0.05). A higher percentage of cases (47%) had not engaged in any physical activity throughout life as compared to controls (19%)[Adjusted OR 3.7 (1.7-7.7)](p<0.001).
CONCLUSIONS: Abdominal obesity and physical inactivity throughout life were associated with low serum adiponectin and breast cancer risk among subjects. Thus, it is essential for Malaysian women to be physically active and achieve a healthy waistline in order to increase serum adiponectin level and reduce breast cancer risk.
OBJECTIVE: To assess the association of premenopausal and postmenopausal breast cancer risk with fat and fat subtypes intake.
METHODOLOGY: This is a population based case-control study conducted in Kuala Lumpur, Malaysia from January 2006 to December 2007. Food intake pattern was collected from 382 breast cancer patients and 382 control group via an interviewer-administered food frequency questionnaire. Logistic regression was used to compute odds ratios (OR) with 95% confidence intervals (CI) and a broad range of potential confounders was included in analysis.
RESULTS: This study showed that both premenopausal and postmenopausal breast cancer risk did not increase significantly with greater intake of total fat [quartile (Q) 4 versus Q1 OR=0.76, 95% CI, 0.23-2.45 and OR=1.36, 95% CI, 0.30-3.12], saturated fat (ORQ4 to Q1=1.43, 95% CI, 0.51-3.98 and ORQ4 to Q1=1.75, 95% CI, 0.62-3.40), monounsaturated fat (ORQ4 to Q1=0.96, 95% CI, 0.34-1.72 and ORQ4 to Q1=1.74, 95% CI, 0.22-2.79), polyunsaturated fat (ORQ4 to Q1=0.64, 95% CI, 0.23-1.73 and ORQ4 to Q1=0.74, 95% CI, 0.39-1.81), n-3 polyunsaturated fat (ORQ4 to Q1=1.10, 95% CI, 0.49-2.48 and ORQ4 to Q1=0.78, 95% CI, 0.28-2.18), n-6 polyunsaturated fat (ORQ4 to Q1=0.67, 95% CI, 0.24-1.84 and ORQ4 to Q1=0.71, 95% CI, 0.29-1.04) or energy intake (ORQ4 to Q1=1.52, 95% CI, 0.68-3.38 and ORQ4 to Q1=2.21, 95% CI, 0.93-3.36).
CONCLUSION: Total fat and fat subtypes were not associated with pre- and postmenopausal breast cancer risk after controlling for age, other breast cancer risk factors and energy intake. Despite the lack of association, the effects of total fat and fat subtypes intake during premenopausal years towards postmenopausal breast cancer risk still warrant investigation.
MATERIALS AND METHODS: An extensive systematic electronic review (PUBMED, CINAHL, PsyINFO and Ovid) and handsearch were carried out to retrieve published articles up to November 2012, using Depression OR Dysthymia AND (Cancer OR Tumor OR Neoplasms as the keywords. Information about the design of the studies, measuring scale, characteristics of the participants, prevalence of depression and its associated factors from the included studies were extracted and summarized.
RESULTS: We identified 32 eligible studies that recruited 10,826 breast cancer survivors. Most were cross-sectional or prospective designed. The most frequent instrument used to screen depression was the Center for Epidemiological Studies for Depression (CES-D, n=11 studies) followed by the Beck Depression Inventory (BDI, n=6 studies) and the Hospital Anxiety and Depression Scale (HADS, n=6 studies). CES-D returned about similar prevalence of depression (median=22%, range=13-56%) with BDI (median=22%, range=17-48%) but higher than HADS (median=10%, range=1-22%). Depression was associated with several socio-demographic variables, cancer-related factors, treatment-related factors, subject psychological factors, lifestyle factors, social support and quality of life.
CONCLUSIONS: Breast cancer survivors are at risk for depression so that detection of associated factors is important in clinical practice.
METHODS: A total of 335,060 women participating in the European Prospective Investigation into Nutrition and Cancer (EPIC) Study, completed a dietary questionnaire from 1992 to 2000, and were followed-up until 2010 for incidence of breast cancer. Hazard ratios (HR) of breast cancer by country-specific, as well as cohort-wide categories of beverage intake were estimated.
RESULTS: During an average follow-up of 11 years, 1064 premenopausal, and 9134 postmenopausal breast cancers were diagnosed. Caffeinated coffee intake was associated with lower risk of postmenopausal breast cancer: adjusted HR=0.90, 95% confidence interval (CI): 0.82 to 0.98, for high versus low consumption; Ptrend=0.029. While there was no significant effect modification by hormone receptor status (P=0.711), linear trend for lower risk of breast cancer with increasing caffeinated coffee intake was clearest for estrogen and progesterone receptor negative (ER-PR-), postmenopausal breast cancer (P=0.008). For every 100 ml increase in caffeinated coffee intake, the risk of ER-PR- breast cancer was lower by 4% (adjusted HR: 0.96, 95% CI: 0.93 to 1.00). Non-consumers of decaffeinated coffee had lower risk of postmenopausal breast cancer (adjusted HR=0.89; 95% CI: 0.80 to 0.99) compared to low consumers, without evidence of dose-response relationship (Ptrend=0.128). Exclusive decaffeinated coffee consumption was not related to postmenopausal breast cancer risk, compared to any decaffeinated-low caffeinated intake (adjusted HR=0.97; 95% CI: 0.82 to 1.14), or to no intake of any coffee (HR: 0.96; 95%: 0.82 to 1.14). Caffeinated and decaffeinated coffee were not associated with premenopausal breast cancer. Tea intake was neither associated with pre- nor post-menopausal breast cancer.
CONCLUSIONS: Higher caffeinated coffee intake may be associated with lower risk of postmenopausal breast cancer. Decaffeinated coffee intake does not seem to be associated with breast cancer.
METHODS: We conducted a fine-mapping analysis in 55,540 breast cancer cases and 51,168 controls from the Breast Cancer Association Consortium.
RESULTS: Conditional analyses identified two independent association signals among women of European ancestry, represented by rs9790517 [conditional P = 2.51 × 10(-4); OR, 1.04; 95% confidence interval (CI), 1.02-1.07] and rs77928427 (P = 1.86 × 10(-4); OR, 1.04; 95% CI, 1.02-1.07). Functional annotation using data from the Encyclopedia of DNA Elements (ENCODE) project revealed two putative functional variants, rs62331150 and rs73838678 in linkage disequilibrium (LD) with rs9790517 (r(2) ≥ 0.90) residing in the active promoter or enhancer, respectively, of the nearest gene, TET2. Both variants are located in DNase I hypersensitivity and transcription factor-binding sites. Using data from both The Cancer Genome Atlas (TCGA) and Molecular Taxonomy of Breast Cancer International Consortium (METABRIC), we showed that rs62331150 was associated with level of expression of TET2 in breast normal and tumor tissue.
CONCLUSION: Our study identified two independent association signals at 4q24 in relation to breast cancer risk and suggested that observed association in this locus may be mediated through the regulation of TET2.
IMPACT: Fine-mapping study with large sample size warranted for identification of independent loci for breast cancer risk.